The dendritic tree of spinal neurons in dogs with experimental hind-limb rigidity.

Abstract

AbstractThe dendritic tree of lumbosacral neurons from dogs with experimental hind‐limb rigidity, produced by temporary lumbosacral ischemia, was reduced to about one‐third of the mean normal size, as previously established in Golgi‐Kopsch preparations. The size reduction was due to the loss only of the more distal segments of the tree by the neurons which survived the ischemic episode, thus decreasing the mean radius of the dendritic projections. The mean number of primary dendrites/neuron remained essentially the same as in the normal but the portions extending beyond about 100 μ from cell body, and all their branches, suffered truncation: the branches originating closer to the cell body suffered the same truncation beyond the 100 μ border. The mean perikaryon size and size range in the sample of 300 neurons from three rigid dogs was not reduced from that of the 360 neuron sample from three normal animals. The loss of nearly two‐thirds of dendrite surface, with consequent loss of all contacts with other neurons normally handled by this major fraction of the dendritic tree, compounded the denervation and isolation sustained by the cell body and surviving proximal part of the tree, due to the marked mortality of interneurons during the ischemic episode. The reduction of the mean of the calculated synaptic endings/neuron for the entire sample to less than one‐fifth of normal and the narrowing of the range of synaptic populations/neuron to one‐seventh of normal are some indications of the magnitude and consequences of this morphological alteration; an alteration concomitant with the demonstrated functional alterations in such neurons. The orderliness of the dendrite organization, as found in the sample of normal neurons, however, did not change to randomness in the altered, „spastic”︁ ones. The peripheral portion of the dendritic arborization failed to survive the denervation and was promptly sloughed, it is postulated, because of its greater vulnerability to denervation, due to a greater dependency upon a continuous transneuronal supply of neurotrophic factors. This dependency may increase exponentially with increasing distance of dendrite segments from cell body. The concept of neuronal interdependence (Gelfan, '64) is extended to include viability of at least part of the dendritic tree.